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1. Introduction
Parkinsonian syndromes are a heterogeneous entity of movement disorders, which can be
subdivided into idiopathic Parkinson’s disease, rare genetic forms of Parkinson’s disease as
well as symptomatic and atypical parkinsonian syndromes. In addition, a number of other
neurodegenerative disorders may show clinical signs of Parkinsonism. The etiology,
histopathology, clinical manifestation and disease course varies significantly among these
disorders. A correct and early differential diagnosis therefore is essential for proper
prognostic estimation and consultancy of the patient as well as a prerequisite for inclusion
in clinical studies.
This chapter will summarize diagnostic criteria mainly focussing on the diagnosis of
idiopathic Parkinson’s disease (iPD) and delineate specific factors to differentiate this
disorder from other disease entities.
2. Clinical signs
Idiopathic Parkinson’s disease is a progressive, neurodegenerative movement disorder,
which in its most classical manifestation is characterized by the triad of bradykinesia,
muscular rigidity and tremor. IPD is the most frequent neurodegenerative movement
disorder with a mean prevalence of ~150/100.000 (Errea et al., 1999; Walker et al., 2010). A
definite diagnosis has to be based on histopathological analysis and requires cell loss in the
substantia nigra, the presence of Lewy bodies, which stain for alpha-synuclein and
ubiquitin, and usually can be obtained only post mortem. In addition, the histology has to
exclude histopathological features of other disorders, which could mimick clinical PD, such
as atypical parkinsonian syndromes (Gelb et al., 1999). While these criteria are useful for
post mortem classification, several attempts have been made to define clinical diagnostic
criteria, e.g. by the UK Parkinson’s Disease Society Brain Bank (UKPDSBB) (Hughes et al.,
1992) or the National Institute of Neurological Disorders and Stroke (NINDS) (Gelb et al.,
1999). For clinical practice, the implementation of modified UKPDSBB criteria has proven
useful: here, the diagnosis is based on (1) the identification of parkinsonian symptoms, (2)
the absence of exclusion criteria and (3) the presence of prospective positive criteria
(Table 1). However, it has to be kept in mind, that even if these criteria are verified by expert
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2 Diagnosis and Treatment of Parkinson’s Disease
neurologists, the diagnostic certainty is only between 75 - 90 % when compared with the
results of the autopsy (Hughes et al., 2001; Dickson et al., 2009).
Step 3 Supportive prospective positive criteria for idiopathic Parkinson’s disease (Three
or more required for diagnosis of definite Parkinson's disease)
- Unilateral onset
- Rest tremor present
- Progressive disorder
- Persistent asymmetry affecting side of onset most
- Excellent response (70-100%) to levodopa
- Severe levodopa-induced chorea
- Levodopa response for 5 years or more
- Clinical course of 10 years or more
Table 1. UK Parkinson’s Disease Society Brain Bank (UKPDSBB) clinical diagnostic criteria
for idiopathic Parkinson’s disease (from (Hughes et al., 1992).
Although numerous supplementary technical exams are available, which may increase
diagnostic certainty, the initial diagnosis remains a clinical one and can be based purely on
medical history and clinical examination. Motor symptoms in iPD are clinically most
striking, but a number of less prominent non-motor symptoms may already be present at
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Diagnosis and Differential Diagnosis of Parkinson’s Disease 3
2.1.1 Bradykinesia
Slowness of initiation and execution of voluntary movements, such as limb movements,
facial expression or gait, characterizes bradykinesia. Diadochokinesis (the ability to perform
rapid alternating movements) is usually slowed (Haaxma et al., 2010). Micrographia with a
characteristic decrease of character size towards the end of the line, the shuffling gait with a
diminished gait quadrangle and reduced arm swing, and hypomimia with a progressive
loss of facial expression are classical manifestations of bradykinesia. Because of the severe
hypomimia with a lack to adequately support emotional expression, PD patients may
wrongly be considered depressive. At the same time, one has to keep in mind that
depression is a common concomitant disorder, which may occur in up to ~ 20 % of PD
patients (Brown et al., 2011).
2.1.2 Tremor
The characteristic tremor is a low-frequency (4-6 Hz) resting tremor, but other tremor forms,
such as an action tremor or a postural tremor may occur as the disease progresses (Jankovic
et al., 1999). Other tremor entities, most importantly essential tremor (ET), have to be
considered in the differential diagnosis and tremor frequency is a major differentiation
criterion (see part 4.4). Therefore, a tremor analysis may be a helpful additional examination
to quantify the characteristics of the tremor presented. There is evidence to suggest that
there is an association and even histopathological overlap in some cases of ET and iPD, but
the case is not yet closed on this issue (Raethjen and Deuschl, 2009). Like most symptoms in
iPD, the tremor manifests with a unilateral preference. In the course of the disease, tremor
intensity may diminish and give way to the bradykinetic symptoms. Very importantly one
has to note, that about one of four of all iPD patients does not develop a characteristic
tremor during the entire course of the disease (Hughes et al., 1993).
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4 Diagnosis and Treatment of Parkinson’s Disease
2.1.3 Rigidity
Rigidity becomes apparent at the clinical examination, when the passive movement of a
limb is impaired by a wax-like resistance. In combination with the tremor frequency this
results in the cogwheel phenomenon upon passive movement in a joint. Many patients with
iPD initially complain of unilateral back and/or shoulder pain as a consequence of the
asymetric muscular tone, which may result in the consultation of an orthopedic specialist
before final referral to a neurologist (Madden and Hall, 2010).
2.2.2 Dysautonomia
Dysautonomic features, such as seborrhoea, orthostatic hypotension, gastrointestinal or
urinary dysfunction may occur before or after the onset of motor symptoms (Bassetti, 2010).
Their early presence (especially urinary dysfunction, orthostatic hypotension) should
however always challenge the diagnosis of iPD and lead to consideration of the differential
diagnosis of atypical parkinsonian syndromes, such as multisystem atrophy (MSA) or
progressive supranuclear palsy (PSP) (Colosimo et al., 2010).
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Diagnosis and Differential Diagnosis of Parkinson’s Disease 5
Urinary dysfunction is especially debilitating for the patient and usually manifests as
overactive bladder syndrome, which has been attributed to the degeneration of central
serotonergic projections. It correlates with disease severity (measured by the UPDRS-III
score) and patient age (Iacovelli et al., 2010).
Gastrointestinal symptoms are present in more than half of iPD patients and may comprise
constipation, dysphagia, nausea, vomiting, incomplete bowel emptying or incontinence. As
for other dysautonomic symptoms, the prevalence in atypical parkinsonian syndromes, such
as MSA or PSP, but also in DLB is much higher (Colosimo et al., 2010).
Symptomatic postural hypotension is less frequent in iPD, but ~20 % of the patients show a
drop in systolic blood pressure of more than 20 mmHg associated with postural events
(Senard et al., 1997). If orthostatic hypotension is prominent at initial presentation, the
diagnosis of MSA should be considered.
While above-mentioned symptoms are likely to be verbalized by the patients, sexual
dysfunction is not. Patients may not even be aware of the fact that erectile dysfunction and
loss of libido are part of the non-motory symptom complex observed in iPD and these
symptoms are therefore likely to be underreported. Nevertheless, a recent study analyzing
the most bothersome symptoms reported by iPD patients in early stage disease (up to 6
years disease duration) listed sexual dysfunction at place 12 of 24 and this was similar in late
stage disease patients (Politis et al., 2010).
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6 Diagnosis and Treatment of Parkinson’s Disease
Autonomic failure
- Gastrointestinal dysfunction
- Urinary dysfunction
- Sexual dysfunction
- Orthostatic hypotension
Sensory deficits
- Olfactory dysfunction
- Pain
Table 2. Non-motor features which may occur in idiopathic Parkinson’s disease.
3. Additional exams
Although the diagnosis of iPD can be made based purely on clinical examination, additional
technical exams can help to differentiate other degenerative disorders, most importantly
secondary or atypical parkinsonian syndromes.
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Diagnosis and Differential Diagnosis of Parkinson’s Disease 7
2010). It remains to be seen whether similar techniques find application in the clinical
practice and whether they will be able to separate other entities from iPD.
Nevertheless, conventional CT and MRI imaging has its place in the diagnostic workup for
suspected iPD and is widely used to exclude common differential diagnoses, such as
vascular PD, Wilson’s disease, or atypical parkinsonian syndromes (see section 4).
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8 Diagnosis and Treatment of Parkinson’s Disease
al., 2006). Due to better sensitivity and the correlation to clinical progression the DaTSCAN
currently may be more suitable in the early diagnosis of iPD than [123I]-MIBG scintigraphy.
SPECT imaging also allows quantifying the postsynaptic dopamine receptor status, which can
be helpful in the differentiation of iPD and atypical parkinsonian syndromes. D2 receptors can
be imaged by application of [123I]-IBZM or [123I]-IBF and are decreased in atypical parkinsonian
syndromes, such as MSA or PSP, but normal or even upregulated in early iPD (Kim et al.,
2002) (Fig. 1b). Imaging techniques aiming at the visualization of cerebral blood flow, such as
[99mTc]-ECD (so-called Neurolite) or FDG, can help in the identification of corticobasal
degeneration, where an asymmetrical reduction of perfusion in cortical areas can be revealed
(Hossain et al., 2003) and discriminate towards PSP (Zhang et al., 2001).
Non-dopaminergic functions are also accessible to PET and SPECT imaging, although these
examinations are not performed routinely. For example, the 11C-WAY100635 PET can
visualize reduced serotonin receptor expression in iPD, which has been suggested to play a
role in iPD-associated depression, and evaluation of 11C-PK11195 binding by PET
examination reflects microglial activation associated with iPD (Brooks, 2007).
Fig. 2. Transcranial B-Mode sonography of the midbrain (purple dotted line). Controls show
little to no hyperechogenicity (white dotted line) in the substantia nigra (a) as compared to
markedly increased hyperechogenicity in iPD patients (b).
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Diagnosis and Differential Diagnosis of Parkinson’s Disease 9
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10 Diagnosis and Treatment of Parkinson’s Disease
iPD (Srulijes et al., 2011). Also, tremor is the symptom, which is most resistant to
dopaminergic therapy and therefore may result only in an insufficient response.
4. Differential diagnosis
In the following part of this chapter, a number of clinically relevant differential diagnoses
are discussed. The main clinical differences are presented along with the appropriate
diagnostic tools for the discrimination against iPD.
Fig. 3. Characteristic MRI findings in PSP and MSA. Thinning of cerebral peduncles
(“Mickey mouse sign”) (a) and mesencephalic atrophy (“hummingbird sign”) (b) on T2-
weighted images in PSP. Cerebellar and pontine atrophy (c), hyperintense putaminal rim (d)
and degeneration of pontocerebellar projections (“hot cross bun sign”) (e) as observed on
T2-weighted images in patients with MSA.
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Diagnosis and Differential Diagnosis of Parkinson’s Disease 11
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12 Diagnosis and Treatment of Parkinson’s Disease
Fig. 4. Characteristic MRI findings in CBD. Asymmetric frontoparietal cortical atrophy with
an emphasis on the central region in a conventional T1-weighted axial section (a), curved
planar reformation or “pancake” representation of the cortex (b) or paramedian sagittal T2-
weighted image (c).
Focal or asymmetric cortical atrophy with a frontoparietal preference may be present on
MRI (Fig. 4) and a corresponding hypoperfusion/hypometabolism may be detected by
SPECT/PET (see section 3.1.2).
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Diagnosis and Differential Diagnosis of Parkinson’s Disease 13
which may be due to the heterogeneity of this disorder as well as a possible coincidence of
vascular changes and iPD. Clinically, patients may present with a slowly progressive difficulty
of gait, while the upper extremities usually are less affected – thus the term “lower-body
parkinsonism”. Tremor is less frequent, but patients may show a multitude of additional
symptoms, such as corticospinal tract signs, pseudobulbar palsy, dementia or incontinence,
depending on the distribution of the microvascular alterations (systematically reviewed in
(Kalra et al., 2010). Rarely, symptoms occur abruptly after an ischemic incidence (Alarcón et
al., 2004). Response to dopaminergic therapy usually is limited.
In contrast to iPD, the native CT scan and the MRI may be helpful in the identification of
vascular lesions and a history of arteriosclerosis, hypertension and other cardiovascular risk
factors may be indicative.
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14 Diagnosis and Treatment of Parkinson’s Disease
The prognosis of drug-induced Parkinsonism is rather good as most patients recover after
discontinuation of medication. If parkinsonian symptoms are not reversible, one should
consider the presence of iPD, which has been unmasked by the anti-dopaminergic medication.
6. Summary
The diagnosis of idiopathic Parkinson’s disease is mainly based on clinical criteria of motor
symptoms, such as bradykinesia, tremor and rigidity.
If these are met, other signs of atypical and secondary parkinsonian syndromes, for example
MSA, PSP, CBD, vascular parkinsonism, NPH or LBD have to be excluded. In addition to
clinical signs typical of these disorders, auxiliary exams, including olfactory testing, MRI
and SPECT imaging can help to identify these entities.
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Diagnosis and Differential Diagnosis of Parkinson’s Disease 15
Finally, the diagnosis of iPD is supported by prospective criteria, which have to be met
during the course of the disease, such as levodopa response, asymmetric symptoms and
disease progression.
There is no single reliable biomarker for iPD available yet and a definite diagnosis currently
can be made only by histology.
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20 Diagnosis and Treatment of Parkinson’s Disease
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Diagnosis and Treatment of Parkinson's Disease
Edited by Prof. Abdul Qayyum Rana
ISBN 978-953-307-465-8
Hard cover, 264 pages
Publisher InTech
Published online 22, September, 2011
Published in print edition September, 2011
Parkinson's disease is diagnosed by history and physical examination and there are no laboratory
investigations available to aid the diagnosis of Parkinson's disease. Confirmation of diagnosis of Parkinson's
disease thus remains a difficulty. This book brings forth an update of most recent developments made in terms
of biomarkers and various imaging techniques with potential use for diagnosing Parkinson's disease. A
detailed discussion about the differential diagnosis of Parkinson's disease also follows as Parkinson's disease
may be difficult to differentiate from other mimicking conditions at times. As Parkinson's disease affects many
systems of human body, a multimodality treatment of this condition is necessary to improve the quality of life of
patients. This book provides detailed information on the currently available variety of treatments for
Parkinson's disease including pharmacotherapy, physical therapy and surgical treatments of Parkinson's
disease. Postoperative care of patients of Parkinson's disease has also been discussed in an organized
manner in this text. Clinicians dealing with day to day problems caused by Parkinson's disease as well as other
healthcare workers can use beneficial treatment outlines provided in this book.
How to reference
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Qayyum Rana (Ed.), ISBN: 978-953-307-465-8, InTech, Available from:
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